Hypoesthesia after an inferior alveolar nerve (IAN) block does not commonly occur, but some cases are reported. The causes of hypoesthesia include a needle injury or toxicity of local anesthetic agents, and the incidence itself can cause stress to both dentists and patients. This case presents a hypoesthesia on mental nerve area followed by IAN block anesthesia with 2% lidocaine. Prescription of steroids for a week was performed and periodic follow up was done. After 1 wk, the symptoms got much better and after 4 mon, hypoesthesia completely disappeared. During this healing period, only early steroid medication was prescribed. In most cases, hypoesthesia is resolved within 6 mon, but being aware of etiology and the treatment options of hypoesthesia is important. Because the hypoesthesia caused by IAN block anesthesia is a mild to moderate nerve injury, early detection of symptom and prescription of steroids could be helpful for improvement of the hypoesthesia.
Anesthesia ; Anesthetics ; Anesthetics, Local ; Dentists ; Follow-Up Studies ; Humans ; Hypesthesia ; Incidence ; Lidocaine ; Mandibular Nerve ; Needles ; Prescriptions ; Steroids

Triple A syndrome is a rare genetic disorder caused by mutations in the achalasia-addisonianism-alacrima syndrome (AAAS) gene which encodes a tryptophan aspartic acid (WD) repeat-containing protein named alacrima-achalasia-adrenal insufficiency neurologic disorder (ALADIN). Northern blot analysis shows that the 2.1 kb AAAS mRNA is expressed in various tissues with stronger expression in testis and pancreas. We show that human ALADIN is a protein with an apparent molecular weight of 60 kDa, and expressed in the adrenal gland, pituitary gland and pancreas. Furthermore, biochemical analysis using anti-ALADIN antibody supports the previous finding of the localization of ALADIN in the nuclear membrane. The mutations S544G and S544X show that alteration of S544 residue affects correct targeting of ALADIN to the nuclear membrane.
Adrenal Insufficiency/*genetics ; Antibodies/immunology ; Cloning, Molecular ; DNA, Complementary/genetics ; Esophageal Achalasia/*genetics ; Gene Expression Profiling ; Hela Cells ; Humans ; Lacrimal Apparatus Diseases/*genetics ; Mutagenesis, Site-Directed ; Nerve Tissue Proteins/*analysis/*genetics/immunology ; Nuclear Pore/chemistry ; Nuclear Pore Complex Proteins/*analysis/*genetics/immunology ; RNA, Messenger/analysis/genetics ; Syndrome ; Tissue Distribution

In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague–Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.